RESUMEN
During times of maternal stress, developing embryos can be exposed to elevated levels of glucocorticoids, which can affect development and permanently alter offspring phenotype. In placental species, the placenta mediates fetal exposure to maternal glucocorticoids via metabolism, yet the placenta itself responds to glucocorticoids to regulate offspring growth and development. In oviparous species, maternal glucocorticoids can be deposited into the egg yolk and are metabolized early in development. This metabolism is mediated by the extraembryonic membranes, but it is unknown if the extraembryonic membranes also respond to maternal glucocorticoids in a way comparable to the placenta. In this study, we quantified the expression of acyl-CoA thioesterase 13 (Acot13) as an initial marker of the membrane's response to corticosterone in chicken (Gallus gallus) eggs. Acot13 regulates fatty acid processing in the embryo, to potentially regulate resource availability during development. We addressed the following questions using Acot13 expression: 1) Do the extraembryonic membranes respond to yolk corticosterone early in development? 2) Is the response to corticosterone dependent on the dose of corticosterone? 3) What is the duration of the response to corticosterone? 4) Does a metabolite of corticosterone (5ß-corticosterone) elicit the same response as corticosterone? We found that corticosterone significantly induces the expression of Acot13 on day four of development and that expression of Acot13 increases with the dose of corticosterone. Further, we found expression of Acot13 is significantly elevated by corticosterone on days four and six of development compared to oil treated eggs, but not on days eight and ten. Although this response is transient, it occurs during a critical period of development and could initiate a cascade of events that ultimately alter offspring phenotype. Finally, we found that 5ß-corticosterone does not increase the expression of Acot13, indicating that metabolism inactivates corticosterone. Ultimately, this study provides insight into the mechanisms underlying how maternally deposited glucocorticoids can affect embryonic development.
Asunto(s)
Corticosterona , Placenta , Animales , Femenino , Embarazo , Corticosterona/farmacología , Corticosterona/metabolismo , Placenta/metabolismo , Glucocorticoides/metabolismo , Aves , Membranas Extraembrionarias/metabolismoRESUMEN
When females experience stress during reproduction, developing embryos can be exposed to elevated levels of glucocorticoids, which can permanently affect offspring development, physiology, and behavior. However, the embryo can regulate exposure to glucocorticoids. In placental species, the placenta regulates embryonic exposure to maternal steroids via metabolism. In a comparable way, recent evidence has shown the extraembryonic membranes of avian species also regulate embryonic exposure to a number of maternal steroids deposited in the yolk via metabolism early in development. However, despite the known effects of embryonic exposure to glucocorticoids, it is not yet understood how glucocorticoids are metabolized early in development. To address this knowledge gap, we injected corticosterone into freshly laid chicken (Gallus gallus) eggs and identified corticosterone metabolites, located metabolomic enzyme transcript expression, tracked metabolomic enzyme transcript expression during the first six days of development, and determined the effect of corticosterone and metabolites on embryonic survival. We found that yolk corticosterone was metabolized before day four of development into two metabolites: 5ß-corticosterone and 20ß-corticosterone. The enzymes, AKR1D1 and CBR1 respectively, were expressed in the extraembryonic membranes. Expression was dynamic during early development, peaking on day two of development. Finally, we found that corticosterone exposure is lethal to the embryos, yet exposure to the metabolites is not, suggesting that metabolism protects the embryo. Ultimately, we show that the extraembryonic membranes of avian species actively regulate their endocrine environment very early in development.
Asunto(s)
Corticosterona , Placenta , Animales , Femenino , Embarazo , Corticosterona/farmacología , Corticosterona/metabolismo , Placenta/metabolismo , Yema de Huevo/metabolismo , Glucocorticoides/metabolismo , Pollos/metabolismo , Esteroides/metabolismoRESUMEN
Although physiological responses to the thermal environment are most frequently investigated using constant temperatures, the incorporation of thermal variability can allow for a more accurate prediction of how thermally sensitive species respond to a rapidly changing climate. In species with temperature-dependent sex determination (TSD), developmental responses to incubation temperature are mediated by several genes involved in gonadal differentiation. Kdm6b and Dmrt1 respond to cool incubation temperatures and are associated with testis development, while FoxL2 and Cyp19A1 respond to warm incubation temperatures and are associated with ovary development. Using fluctuating incubation temperatures, we designed two studies, one investigating how conflicting thermal cues affect the timing of commitment to gonadal development, and another investigating the rapid molecular responses to conflicting thermal cues in the red-eared slider turtle (Trachemys scripta). Using gene expression as a proxy of timing of commitment to gonadal fate, results from the first study show that exposure to high amounts of conflicting thermal cues during development delays commitment to gonadal fate. Results from the second study show that Kdm6b splice variants exhibit differential responses to early heat wave exposure, but rapidly (within 2â days) recover to pre-exposure levels after the heat wave. Despite changes in the expression of Kdm6b splice variants, there was no effect on Dmrt1 expression. Collectively, these findings demonstrate how short exposures to heat early in development can change how embryos respond to heat later in development.
Asunto(s)
Calor , Tortugas , Animales , Masculino , Femenino , Procesos de Determinación del Sexo , Tortugas/fisiología , Diferenciación Sexual , TemperaturaRESUMEN
Predation or brood parasitism risks can change the behaviors and reproductive decisions in many parental animals. For oviparous species, mothers can mitigate their reproductive success in at least three ways: (1) by avoiding nest sites with high predation or parasitism risks, (2) through hormonal maternal effects that developmentally prime offspring for survival in risky environments, or (3) by investing less in reproduction when predation or parasitism risks are high. Here, we tested if perceived predation and parasitism risks can induce any of these behavioral or physiological responses by exposing female red-winged blackbirds (Agelaius phoeniceus) to playbacks of two major nest threats, a predator (Cooper's hawk, Accipiter cooperii) and an obligate brood parasite (brown-headed cowbird; Molothrus ater), as well as two controls (harmless Eastern meadowlark, Sturnella magna; and silence). We found that female blackbirds did not avoid nesting at sites treated with predator or brood parasite playbacks, nor were females more likely to abandon nesting attempts at these sites. Egg size and yolk hormone profiles, which are common proxies for maternal investment in oviparous species, were statistically similar across treatment sites. Instead, we found intraclutch variation in yolk steroid hormone profiles: concentrations of three progestogens (pregnanedione, 17α-hydroxypregnenolone, and deoxycorticosterone) and two androgens (testosterone and androstenedione) were higher in third-laid than first-laid eggs. Our study largely confirms previous findings of consistent intraclutch yolk hormone variation in this species, in birds in general, and in other oviparous lineages, but uniquely reports on several yolk steroid hormones largely overlooked in the literature on hormone-mediated maternal effects.
Asunto(s)
Parásitos , Passeriformes , Pájaros Cantores , Animales , Femenino , Masculino , Conducta Predatoria , Herencia Materna , Pájaros Cantores/fisiología , Passeriformes/fisiología , Testosterona , Comportamiento de Nidificación/fisiologíaRESUMEN
Maternal stress during reproduction can influence how offspring respond to stress later in life. Greater lifetime exposure to glucocorticoid hormones released during stress is linked to greater risks of behavioral disorders, disease susceptibility, and mortality. The immense variation in individual's stress responses is explained, in part, by prenatal glucocorticoid exposure. To explore the long-term effects of embryonic glucocorticoid exposure, we injected Japanese quail (Coturnix japonica) eggs with corticosterone. We characterized the endocrine stress response in offspring and measured experienced aggression at three different ages. We found that prenatal glucocorticoid exposure affected (1) the speed at which the stress response was terminated suggesting dysregulated negative feedback, (2) baseline corticosterone levels in a manner dependent on current environmental conditions with higher levels of experienced aggression associated with higher levels of baseline corticosterone, (3) the magnitude of an acute stress response based on baseline concentrations. We finish by proposing a framework that can be used to test these findings in future work. Overall, our findings suggest that the potential adaptive nature of prenatal glucocorticoid exposure is likely dependent on environmental context and may also be tempered by the negative effects of longer exposure to glucocorticoids each time an animal faces a stressor.
Asunto(s)
Glucocorticoides , Efectos Tardíos de la Exposición Prenatal , Animales , Femenino , Humanos , Glucocorticoides/efectos adversos , Corticosterona , Coturnix/fisiología , Reproducción/fisiología , Estrés PsicológicoRESUMEN
Variation in developmental conditions can affect a variety of embryonic processes and shape a number of phenotypic characteristics that can affect offspring throughout their lives. This is particularly true of oviparous species where development typically occurs outside of the female, and studies have shown that traits such as survival and behavior can be altered by both temperature and exposure to steroid hormones during development. In species with temperature-dependent sex determination (TSD), the fate of gonadal development can be affected by temperature and by maternal estrogens present in the egg at oviposition, and there is evidence that these factors can affect gene expression patterns. Here, we explored how thermal fluctuations and exposure to an estrogen metabolite, estrone sulfate, affect the expression of several genes known to be involved in sexual differentiation: Kdm6b, Dmrt1, Sox9, FoxL2 and Cyp19A1. We found that most of the genes responded to both temperature and estrone sulfate exposure, but that the responses to these factors were not identical, in that estrone sulfate effects occur downstream of temperature effects. Our findings demonstrate that conjugated hormones such as estrone sulfate are capable of influencing temperature-dependent pathways to potentially alter how embryos respond to temperature, and highlight the importance of studying the interaction of maternal hormone and temperature effects.
Asunto(s)
Procesos de Determinación del Sexo , Tortugas , Animales , Estrona/análogos & derivados , Estrona/metabolismo , Femenino , Expresión Génica , Hormonas , Procesos de Determinación del Sexo/genética , Diferenciación Sexual/fisiología , Temperatura , Tortugas/fisiologíaRESUMEN
The thermal environment that organisms experience can affect many aspects of their phenotype. As global temperatures become more unpredictable, it is imperative that we understand the molecular mechanisms by which organisms respond to variable, and often transient, thermal environments. Beyond deciphering the mechanisms through which organisms respond to temperature, we must also appreciate the underlying variation in temperature-dependent processes, as this variation is essential for understanding the potential to adapt to changing climates. In this Commentary, we use temperature-dependent sex determination as an example to explore the mechanistic processes underlying the development of temperature-sensitive phenotypes. We synthesize the current literature on how variable thermal conditions affect these processes and address factors that may limit or allow organisms to respond to variable environments. From these examples, we posit a framework for how the field might move forward in a more systematic way to address three key questions: (1) which genes directly respond to temperature-sensitive changes in protein function and which genes are downstream, indirect responders?; (2) how long does it take different proteins and genes to respond to temperature?; and (3) are the experimental temperature manipulations relevant to the climate the organism experiences or to predicted climate change scenarios? This approach combines mechanistic questions (questions 1 and 2) with ecologically relevant conditions (question 3), allowing us to explore how organisms respond to transient thermal environments and, thus, cope with climate change.
Asunto(s)
Adaptación Fisiológica , Cambio Climático , Fenotipo , TemperaturaRESUMEN
Maternal hormones can shape offspring development and increase survival when predation risk is elevated. In songbirds, yolk androgens influence offspring growth and begging behaviors, which can help mitigate offspring predation risk in the nest. Other steroids may also be important for responding to nest predation risk, but non-androgen steroids have been poorly studied. We used a nest predator playback experiment and liquid chromatography with tandem mass spectrometry (LC-MS-MS) to assess whether nest predation risk influences deposition of 10 yolk steroids. We found no clear evidence that yolk androgen deposition changed when perception of nest predation risk was experimentally increased. However, elevated nest predation risk led to decreased yolk progesterone deposition. Overall, our results suggest yolk progesterone may be more important than yolk androgens in responses to offspring predation risk and highlight new avenues for research.
Asunto(s)
Pájaros Cantores , Andrógenos , Animales , Comportamiento de Nidificación/fisiología , Conducta Predatoria/fisiología , Progesterona , Pájaros Cantores/fisiología , EsteroidesRESUMEN
There is ample research demonstrating that temperature can have complex effects on biological processes, including the timing of when organisms respond to temperature; some responses occur rapidly while others require an extended exposure time. However, most of what we know about temperature effects comes from studies using constant temperature conditions, which are not reflective of natural, fluctuating temperatures. Species with temperature-dependent sex determination (TSD) present an ideal system to study the temporal aspects of the temperature response because prior research has established a number of temperature-responsive genes involved in TSD, albeit under constant temperatures. To investigate potential differences in timing of sexual development between constant and fluctuating incubation temperatures, we exposed Trachemys scripta embryos to two conditions that produce males (constant 26°C and 26 ± 3°C) and two that produce females (constant 31°C and 31 ± 3°C), and sampled embryonic gonads for gene expression analysisvia qPCR. We analyzed three genes involved in testis differentiation (Kdm6b,Dmrt1, andSox9) and two genes involved in ovary differentiation (Foxl2andCyp19A1). Results show that Kdm6b expression was significantly lower under fluctuating temperatures compared to constant temperatures. Foxl2 and Cyp19A1 expression were also lower under fluctuating temperatures, but not at all stages of development. These results suggest that constant temperatures caused increases in both Foxl2 and Cyp19A1 expression earlier (developmental stage 20) than fluctuating temperatures (stages 22 and 23). Dmrt1 and Sox9 expression did not differ between constant and fluctuating temperatures. These results highlight that not all genes in a temperature-dependent process respond to temperature in the same manner. Whether there are functional consequences of this variation remains to be determined.
Asunto(s)
Procesos de Determinación del Sexo , Tortugas , Animales , Femenino , Expresión Génica , Gónadas , Masculino , Procesos de Determinación del Sexo/genética , Temperatura , Tortugas/fisiologíaRESUMEN
Variation in nestling growth and survival is often influenced by hatching order, with first-hatched offspring having an advantage over later-hatched younger siblings. In house wrens (Troglodytes aedon), this effect of hatching order is especially evident in asynchronously hatched broods and can lead to sex-specific differences in the size and condition of nestlings. Females appear to allocate the sex of their offspring across the laying order to capitalize on these differences. We hypothesized that levels of circulating corticosterone, the primary metabolic hormone in birds, mediates these sex-specific effects in nestlings. We predicted that: i) baseline levels of corticosterone in nestlings should vary along the hatching order, ii) effects of hatching order on baseline corticosterone should be sex specific, and iii) any sex-specificity of hatching order on baseline corticosterone could be contingent on the degree of hatching synchrony. We tested these predictions in a study in which we measured baseline corticosterone in first- and last-hatched nestlings in synchronously and asynchronously hatching broods. To assess whether any differences in nestling baseline corticosterone levels could be attributed to pre-natal maternal effects, the post-natal environment, or both, we conducted two additional studies in which we measured i) yolk corticosterone in first- and last-laid eggs and ii) baseline corticosterone in nestlings that were cross-fostered to create simulated 'asynchronously' hatched broods. There was a significant interaction between sex and relative hatching order in their effects on nestling baseline corticosterone, but no effect of hatching synchrony. Corticosterone levels remained relatively constant across the hatching order in males but decreased in females. There was a significant effect of laying order on yolk corticosterone, with first-laid eggs containing significantly higher levels of yolk corticosterone than last-laid eggs. Cross-fostering of nestlings at different points of development had no significant effect on nestling corticosterone levels. These results indicate that sex-dependent differences in corticosterone levels across the hatching order may arise, at least in part, from embryonic exposure to maternally derived corticosterone, whereas the post-natal rearing environment plays, at best, a minimal role in determining nestling baseline corticosterone levels.
Asunto(s)
Corticosterona , Pájaros Cantores , Animales , Femenino , MasculinoRESUMEN
Exposure to maternally derived steroids during embryonic development can elicit phenotypic effects in the resulting offspring. Studies of maternal steroid effects, especially rich in mammals and birds, have offered exciting insights into the evolution of maternal effects in vertebrates. To extend this literature, we quantified levels of steroids in the eggs of four neotropical dendrobatid frogs that lay terrestrial clutches, a reproductive strategy that has evolved multiple times in amphibians. Building on our observational results, we then manipulated levels of pregnenolone and progesterone in eggs of one species and examined how this affected steroid levels during development. Eggs of all four species had detectable steroids levels, with progestogens being more abundant than androgens and glucocorticoids. Estrogens could not be detected. Immersion of frog eggs in a solution containing pregnenolone and progesterone resulted in elevated levels of both steroids early in development, but levels declined and were similar to those in unmanipulated eggs by the end of development. Treated eggs also exhibited a transient increase in levels of steroids that can be produced from pregnenolone and progesterone. Overall, our findings demonstrate that frog eggs contain steroids similar to what has been observed in other egg-laying vertebrates. During development, steroid levels are dynamic, further suggesting developing embryos regulate exposure to maternal steroids. These results set the stage for investigating the causes and consequences of maternal steroid effects in frogs.
Asunto(s)
Yema de Huevo , Progesterona , Animales , Anuros , Mamíferos , Herencia Materna , Pregnenolona/farmacología , EsteroidesRESUMEN
Animals with temperature-dependent sex determination (TSD) respond to thermal cues during early embryonic development to trigger gonadal differentiation. TSD has primarily been studied using constant temperature incubations, where embryos are exposed to constant male- or female-producing temperatures, and these studies have identified genes that display sex-specific expression in response to incubation temperature. Kdm6b, a histone demethylase gene, has received specific attention as it is among the initial genes to respond to incubation temperature and is necessary for testis development. Interestingly, Kdm6b retains an intron when eggs are incubated at a constant male-producing temperature, but the role of thermal variability in this developmental process is relatively understudied. Species with TSD regularly experience thermal cues that fluctuate between male- and female-producing temperatures throughout development but it is unclear how Kdm6b responds to such variable temperatures. In this study, we investigate temperature-sensitive splicing in Kdm6b by exposing embryos to male- and female-producing thermal conditions. We show a rapid decrease in levels of the intron retaining transcript of Kdm6b upon exposure to female-producing conditions. These results demonstrate that, under ecologically relevant conditions, temperature-sensitive splicing can differentially regulate genes critical to TSD.
Asunto(s)
Procesos de Determinación del Sexo , Tortugas , Animales , Femenino , Gónadas , Intrones , Masculino , Procesos de Determinación del Sexo/genética , TemperaturaRESUMEN
In species with temperature-dependent sex determination (TSD), incubation temperatures regulate the expression of genes involved in gonadal differentiation and determine whether the gonads develop into ovaries or testes. For most species, natural incubation conditions result in transient exposure to thermal cues for both ovarian and testis development, but how individuals respond to this transient exposure varies and can drive variation in the resulting sex ratios. Here, we argue that variation in the timing to respond to temperature cues, or thermal responsiveness, is a trait needing further study. Recent work in the red-eared slider turtle (Trachemys scripta) has found that when embryos experience transient exposure to warm conditions (i.e., heatwaves), some embryos show high responsiveness, requiring only short exposures to commit to ovarian development, while others show low responsiveness, developing testes even after more extended exposures to warm conditions. We discuss how maternal estrogens might influence thermal responsiveness for organisms that develop under thermal fluctuations. Examining the interplay of molecular responses to more subtle thermal and endocrine environments may reveal significant insights into the process of sex determination in species with TSD.
Asunto(s)
Estrógenos , Tortugas , Animales , Femenino , Gónadas/metabolismo , Masculino , Procesos de Determinación del Sexo/genética , Diferenciación Sexual/genética , Temperatura , Tortugas/genéticaRESUMEN
Most organisms are exposed to bouts of warm temperatures during development, yet we know little about how variation in the timing and continuity of heat exposure influences biological processes. If heat waves increase in frequency and duration as predicted, it is necessary to understand how these bouts could affect thermally sensitive species, including reptiles with temperature-dependent sex determination (TSD). In a multi-year study using fluctuating temperatures, we exposed Trachemys scripta embryos to cooler, male-producing temperatures interspersed with warmer, female-producing temperatures (heat waves) that varied in either timing during development or continuity and then analysed resulting sex ratios. We also quantified the expression of genes involved in testis differentiation (Dmrt1) and ovary differentiation (Cyp19A1) to determine how heat wave continuity affects the expression of genes involved in sexual differentiation. Heat waves applied during the middle of development produced significantly more females compared to heat waves that occurred just 7 days before or after this window, and even short gaps in the continuity of a heat wave decreased the production of females. Continuous heat exposure resulted in increased Cyp19A1 expression while discontinuous heat exposure failed to increase expression in either gene over a similar time course. We report that even small differences in the timing and continuity of heat waves can result in drastically different phenotypic outcomes. This strong effect of temperature occurred despite the fact that embryos were exposed to the same number of warm days during a short period of time, which highlights the need to study temperature effects under more ecologically relevant conditions where temperatures may be elevated for only a few days at a time. In the face of a changing climate, the finding that subtle shifts in temperature exposure result in substantial effects on embryonic development becomes even more critical.
Asunto(s)
Calor , Procesos de Determinación del Sexo , Tortugas/fisiología , Animales , Cambio Climático , Embrión no Mamífero , Femenino , Regulación del Desarrollo de la Expresión Génica , Masculino , Fenotipo , Diferenciación Sexual , Razón de MasculinidadRESUMEN
Predation often has consistent effects on prey behavior and morphology, but whether the physiological mechanisms underlying these effects show similarly consistent patterns across different populations remains an open question. In vertebrates, predation risk activates the hypothalamic-pituitary-adrenal (HPA) axis, and there is growing evidence that activation of the maternal HPA axis can have intergenerational consequences via, for example, maternally-derived steroids in eggs. Here, we investigated how predation risk affects a suite of maternally-derived steroids in threespine stickleback eggs across nine Alaskan lakes that vary in whether predatory trout are absent, native, or have been stocked within the last 25 years. Using liquid chromatography coupled with mass spectroscopy (LC-MS/MS), we detected 20 steroids within unfertilized eggs. Factor analysis suggests that steroids covary within and across steroid classes (i.e. glucocorticoids, progestogens, sex steroids), emphasizing the modularity and interconnectedness of the endocrine response. Surprisingly, egg steroid profiles were not significantly associated with predator regime, although they were more variable when predators were absent compared to when predators were present, with either native or stocked trout. Despite being the most abundant steroid, cortisol was not consistently associated with predation regime. Thus, while predators can affect steroids in adults, including mothers, the link between maternal stress and embryonic development is more complex than a simple one-to-one relationship between the population-level predation risk experienced by mothers and the steroids mothers transfer to their eggs.
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Óvulo/metabolismo , Conducta Predatoria , Smegmamorpha/fisiología , Esteroides/metabolismo , Alaska , Animales , Cromatografía Liquida , Femenino , Lagos , Óvulo/fisiología , Esteroides/análisis , Espectrometría de Masas en TándemRESUMEN
Maternal transfer of steroids to eggs can elicit permanent effects on offspring phenotype. Although testosterone was thought to be a key mediator of maternal effects in birds, we now know that vertebrate embryos actively regulate their exposure to maternal testosterone through steroid metabolism, suggesting testosterone metabolites, not testosterone, may elicit the observed phenotypic effects. To address the role steroid metabolism plays in mediating yolk testosterone effects, we used European starling (Sturnus vulgaris) eggs to characterize the timing of testosterone metabolism and determine whether etiocholanolone, a prominent metabolite of testosterone in avian embryos, is capable of affecting early embryonic development. Tritiated testosterone was injected into freshly laid eggs to characterize steroid movement and metabolism during early development. Varying levels of etiocholanolone were also injected into eggs, with incubation for either 3 or 5 days, to test whether etiocholanolone influences the early growth of embryonic tissues. The conversion of testosterone to etiocholanolone was initiated within 12â h of injection, but the increase in etiocholanolone was transient, indicating that etiocholanolone is also subject to metabolism, and that exposure to maternal etiocholanolone is limited to a short period during early development. Exogenous etiocholanolone manipulation had no significant effect on the growth rate of the embryos or extra-embryonic membranes early in development. Thus, the conversion of testosterone to etiocholanolone may be an inactivation pathway that buffers the embryo from maternal steroids, with any effects of yolk testosterone resulting from testosterone that escapes metabolism; alternatively, etiocholanolone may influence processes other than growth or take additional time to manifest.
Asunto(s)
Desarrollo Embrionario/efectos de los fármacos , Etiocolanolona/farmacología , Estorninos/embriología , Testosterona/metabolismo , Animales , Yema de Huevo/metabolismo , Embrión no Mamífero/metabolismo , Etiocolanolona/metabolismo , Membranas Extraembrionarias/efectos de los fármacos , Femenino , Estorninos/metabolismo , TritioRESUMEN
The steroid 17ß-estradiol (herein "estradiol") is a potent regulator of sexual differentiation that exerts wide-ranging effects on the developing brain and other tissues. The developing gonads are an important source of estradiol but most, if not all, vertebrate embryos are also exposed to maternally derived estradiol during development. In birds, this maternally derived estradiol is present in the egg at the time of oviposition but very little is known about how this source of estradiol influences development. A critical aspect of understanding yolk estradiol effects is deciphering how steroid metabolism may regulate embryonic exposure to yolk estradiol. In this study, we examine the metabolic fate of estradiol during the first five days of incubation in chicken (Gallus gallus) eggs. Using tritiated estradiol to trace the movement and metabolism of estradiol, we demonstrate that estradiol is metabolized to estrone, which is subsequently conjugated to estrone sulfate as the primary metabolite. Estrone sulfate then accumulates in the albumen by day five of incubation. Overall, these findings have important implications for how yolk estradiol may influence development and alter offspring phenotype. Mechanisms through which estradiol, as well as estrone sulfate, might elicit effects are discussed.
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Embrión de Pollo/metabolismo , Yema de Huevo/metabolismo , Desarrollo Embrionario/fisiología , Estradiol/metabolismo , Estrona/análogos & derivados , Animales , Pollos/metabolismo , Yema de Huevo/fisiología , Estrona/metabolismo , Femenino , Masculino , Oviposición/fisiología , FenotipoRESUMEN
Acute rises in glucocorticoid hormones allow individuals to adaptively respond to environmental challenges but may also have negative consequences, including oxidative stress. While the effects of chronic glucocorticoid exposure on oxidative stress have been well characterized, those of acute stress or glucocorticoid exposure have mostly been overlooked. We examined the relationship between acute stress exposure, glucocorticoids and oxidative stress in Japanese quail (Coturnix japonica). We (i) characterized the pattern of oxidative stress during an acute stressor in two phenotypically distinct breeds; (ii) determined whether corticosterone ingestion, in the absence of acute stress, increased oxidative stress, which we call glucocorticoid-induced oxidative stress (GiOS); and (iii) explored how prior experience to stressful events affected GiOS. Both breeds exhibited an increase in oxidative stress in response to an acute stressor. Importantly, in the absence of acute stress, ingesting corticosterone caused an acute rise in plasma corticosterone and oxidative stress. Lastly, birds exposed to no previous acute stress or numerous stressful events had high levels of GiOS in response to acute stress, while birds with moderate prior exposure did not. Together, these findings suggest that an acute stress response results in GiOS, but prior experience to stressors may modulate that oxidative cost.